Evidence map›Paper›PMID 18849970›Full record

ArticleNature2008

DNA double-strand breaks activate a multi-functional genetic program in developing lymphocytes.

Andrea L Bredemeyer, Beth A Helmink, Cynthia L Innes, Boris Calderon, Lisa M McGinnis, Grace K Mahowald, Eric J Gapud, Laura M Walker, Jennifer B Collins, Brian K Weaver and 7 more

Abstract read
In one paragraph

Article in Nature, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

106 citing papers in PubMed, 146 citations in OpenAlex.

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  20. Nemo-Dependent, ATM-Mediated Signals from RAG DNA Breaks atJournal of immunology (Baltimore, Md. : 1950) · 2022
    Article

46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 3 countries.

Andrea L BredemeyerDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Beth A Helmink
Cynthia L Innes
Boris Calderon
Lisa M McGinnis
Grace K Mahowald
Eric J Gapud
Laura M Walker
Jennifer B Collins
Brian K Weaver
Laura Mandik-Nayak
Robert D Schreiber
Paul M Allen
Michael J May
Richard S Paules
Craig H Bassing
Barry P Sleckman
Washington University in St. Louis · USNational Institute of Environmental Health Sciences · USChildren's Hospital of Philadelphia · USUniversity of Veterinary Medicine · HU

Funding

THE V(D)J RECOMBINATION REACTION AND ITS IMPACT ON LYMPHOCYTE DEVELOPMENTR01AI047829 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI SLECKMAN, BARRY P · 2000 to 2021
$7.0M
Molecular Pathways in Suppression and Development of T Lineage LymphomasR01CA125195 · NCI · CHILDREN'S HOSP OF PHILADELPHIA · PI BASSING, CRAIG H · 2007 to 2011
$1.6M
NCI NIH HHS R01 CA125195NIAID NIH HHS R01 AI047829
6 · The paper itself

Abstract

DNA double-strand breaks are generated by genotoxic agents and by cellular endonucleases as intermediates of several important physiological processes. The cellular response to genotoxic DNA breaks includes the activation of transcriptional programs known primarily to regulate cell-cycle checkpoints and cell survival. DNA double-strand breaks are generated in all developing lymphocytes during the assembly of antigen receptor genes, a process that is essential for normal lymphocyte development. Here we show that in murine lymphocytes these physiological DNA breaks activate a broad transcriptional program. This program transcends the canonical DNA double-strand break response and includes many genes that regulate diverse cellular processes important for lymphocyte development. Moreover, the expression of several of these genes is regulated similarly in response to genotoxic DNA damage. Thus, physiological DNA double-strand breaks provide cues that can regulate cell-type-specific processes not directly involved in maintaining the integrity of the genome, and genotoxic DNA breaks could disrupt normal cellular functions by corrupting these processes.

Indexed as

DNA Breaks, Double-StrandedAnimalsAtaxia Telangiectasia Mutated ProteinsB-LymphocytesCell Cycle ProteinsCell LineDNA-Binding ProteinsEnzyme InhibitorsGene Expression ProfilingGene Expression Regulation, DevelopmentalHomeodomain ProteinsMiceMice, KnockoutMice, SCIDNF-kappa BProtein Serine-Threonine KinasesAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Binding ProteinsEnzyme InhibitorsHomeodomain ProteinsNF-kappa BProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID18849970
PMCPMC2605662
OpenAlexW2084253472

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.